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Scientists at the University of Geneva (UNIGE) and Geneva University Hospitals (HUG) have shed light on the far-reaching consequences of maternal obesity, particularly its role in predisposing unborn children to liver diseases and potentially liver cancer.

Obesity, an epidemic looming large in many developed nations, not only poses a significant threat to individual health but also raises concerns about its impact on future generations. Published in JHEP Reports, the study aims to explain the extent to which maternal obesity influences the development of diseases in offspring.

“We wanted to understand whether the children of mothers suffering from obesity were at greater risk of developing liver diseases, and by what biological mechanisms,” said Christian Toso, professor at the UNIGE Faculty of Medicine and senior author, expressing the significance of the study.

According to the researchers, despite the declining prevalence of liver cancer attributed to viral infections, obesity-related liver diseases are steadily on the rise, revealing the need for deeper investigation into their origins and implications. “While the risk of liver cancer due to a hepatic virus is decreasing, obesity-related liver diseases are constantly on the rise,” Toso emphasized, underlining the urgency of addressing this emerging health challenge.

The study involved two groups of female mice: one fed with a high-fat, high-sugar diet mimicking junk food consumption, leading to obesity, and another group fed a standard diet serving as the control.

“At 20 weeks, which corresponds to adulthood in humans, we could not detect any notable differences,” explained Beat Moeckli, junior staff surgeon and researcher in professor Toso’s team and the first author of the study.

However, by 40 weeks, a senior age in mice, significant disparities in liver health emerged, with offspring born to obese mothers exhibiting heightened indicators of liver disease.

Furthermore, upon administering a hepatic carcinogen (Diethylnitrosamine) post-weaning, mice born to obese mothers displayed an alarming 80 percent risk of developing liver cancer compared to 20 percent in the control group. “The mother’s obesity thus has an impact long after the birth of its offspring, which seem to inherit a dysfunctional microbiota despite their own living conditions,” Moeckli said.

Central to these findings is the role of the microbiota, the diverse community of microorganisms living in the gut. “We see a clear effect of the microbiota on the risk of developing liver cancer, indicating its central role in transmitting the risk of disease from mother to child,” Moeckli concluded, highlighting the important role of microbiota in reducing the risk of liver cancer.

While these findings offer valuable insights into the interplay between maternal obesity, microbiota, and liver health, the applicability to humans requires further investigation. Nonetheless, the identification of microbiota as a modifiable factor opens doors to potential therapeutic interventions, such as probiotics, offering hope for easing the adverse effects of maternal obesity on offspring health.

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